Intestinal ECs not only act as a ph

Intestinal ECs not only act as a physiological barrier, but also take
part in the immunological function of the intestine by the formation of
secretary form of immunoglobulin leading to the secretion of IgA and
IgM into the intestinal lumen [1]. Reciprocally, IgG, which is involved
in the antigen transport system, is transported from the intestinal
lumen via the neonatal Fc receptor (FcRn) expressed on the apical
surface of ECs [32]. In addition, ECs release exosomes containing
antigen bound to MHC class II. The released MHC-bound antigen is
thought to induce tolerance, not activation, of antigen-specific T cell
responses [33]. This system might be important aspect of the gut
immune system for the creation of immunologically quiescence
condition at the harsh environment of intestine.
Among ECs in the villous epithelium, we identified M cells sharing
similar characteristic with the M cells originally found in the FAE of
PPs (or PP M cells) and termed them villous M cells [34]. Villous M
cells are thus morphologically similar to M cells in the PPs and are recognized by UEA-1 lectin and M cell-specific NKM16-2-4 antibody, a
marker of murine M cells. The specificity for UAE-1 and NKM 16-2-4
antibody suggests that villousMcellsmost likely harbor identicalα(1,2)
fucose based glycosylation molecules. Like M cells, villous M cells were
capable of taking up Salmonella, Yersinia, and Escherichia coli expressing
invasin. In addition, they are found in villous epithelium in PP-deficient
mice, which allow them to still induce antigen-specific IgA responses
[15,16]. Thus, villous M cells are an alternative antigen-sampling site
and can be consider as the additional targeting site for oral vaccine
delivery.
We recently reported that M cell-like α(1,2) fucose based
glycosylation can be induced on intestinal ECs by environmental
stimuli such as colonization with commensal biota, treatment with
cholera toxin, or treatment with dextran sodium sulfate and termed
these cells as fucosylated ECs (F-ECs) [35]. Although a functional role
of F-ECs in the induction of immune responses against intestinal
antigens needs further investigation, these findings suggest additional
possible strategies to induce F-ECs for the enrichment of antigensampling
system at the intestinal epithelium to vaccine administered
via oral route.

結果 (中文) 1:

肠道 ECs 不仅作为生理屏障，而且还采取所形成的肠道免疫功能部分免疫球蛋白 IgA 分泌导致司形式和IgM 成小肠腔内 [1]。反过来，IgG，涉及在抗原运输系统中，从小肠传输通过新生儿 Fc 受体 (FcRn) 表达对根尖腔表面的 ECs [32]。此外，ECs 释放外泌体包含抗原绑定到 MHC II 类。发布的绑定 MHC 抗原是认为诱导耐受，没有激活的抗原特异性 T 细胞答复 [33]。这个系统可能是肠道的重要方面免疫系统的免疫沉寂创作在小肠的苛刻环境条件。中内皮细胞在具长柔毛的上皮细胞，我们确定了 M 细胞共享与最初发现的 FAE M 细胞相似的特征聚苯硫醚 （或 PP M 细胞） 和所谓的那些具长柔毛 M 细胞 [34]。具长柔毛 M细胞是因此形态类似 M 细胞在聚苯硫醚和东安格利亚大学 1 凝集素及 M 细胞特异性 NKM16-2-4 抗体，均承认小鼠 M 细胞的标记。特异性为阿联酋 1 和恩凯 16-2-4抗体表明，villousMcellsmost 可能港 identicalα(1,2)岩藻糖基于糖基化分子。像 M 细胞，具长柔毛 M 细胞的能占用沙门氏菌、 耶尔森氏菌和大肠埃希氏大肠杆菌表达的侵袭。此外，他们是在 PP 缺绒毛上皮细胞中发现小鼠，允许他们仍然诱导抗原特异性 IgA 反应[15，16].因此，具长柔毛 M 细胞是替代性的抗原采样点可以考虑作为口服疫苗的额外目标站点交付。我们最近报道，M 细胞样 α(1,2) 岩藻糖的基础糖基化可诱导肠 ECs 在环境刺激，如殖民化与共生的生物群，与治疗霍乱毒素或葡聚糖硫酸酯钠盐治疗，称为这些细胞作为岩藻 ECs (F-ECs) [35]。虽然功能的作用F-内皮细胞对肠道的免疫反应的诱导抗原需要进一步调查，这些发现表明附加可能的策略，以促使 F ECs 为丰富的 antigensampling在接种疫苗对肠上皮细胞系统通过口服。

結果 (中文) 3:

肠内皮细胞不仅作为一种生理障碍，也要部分在肠道的免疫功能的形成免疫球蛋白导致IgA分泌形成和秘书IgM进入肠腔[ 1 ]。同样地，IgG，这是涉及在抗原转运系统中，是从肠道输送的通过新生儿Fc受体（FcRn）上腔顶端表达ECS [ 32 ]面。此外，内皮细胞释放其含有结合抗原的MHC II类。释放的MHC结合的抗原是认为诱导免疫耐受，不激活抗原特异性T细胞回应[ 33 ]。这个系统可能是肠道的一个重要方面为建立免疫系统的免疫状态在恶劣环境下的条件。ECS在绒毛上皮细胞中，我们确定了M细胞共享与最初发现在FAE的M细胞相似的特征聚苯硫醚（或PP M细胞）和所谓的那些绒毛M细胞[ 34 ]。绒毛状M细胞在PPS从而M细胞形态相似，通过UEA-1凝集素和M细胞的特定的nkm16-2-4抗体识别，一小鼠M细胞标记物。对于uae-1和NKM 16-2-4特异性抗体表明villousmcellsmost可能拥有相同的α（1,2）基于分子岩藻糖基化。像M细胞，绒毛M细胞能够以沙门氏菌、耶尔森菌，和大肠杆菌中的表达侵袭。此外，他们被发现在绒毛上皮细胞在聚丙烯缺乏老鼠，这让他们还诱导抗原特异性IgA反应[15,16]。因此，绒毛M细胞是一种替代的抗原采样点可以考虑作为口服疫苗的附加靶点交货。我们最近报道，M细胞样α（1,2）岩藻糖基糖基化可诱导内皮细胞的肠道环境刺激如共生生物定植，治疗霍乱毒素，或用葡聚糖硫酸钠治疗，并称之为这些细胞岩藻糖基化的ECS（F-ECS）[ 35 ]。虽然功能作用在对肠道免疫反应的诱导F-ECS抗原需要进一步的调查，这些研究结果表明额外的可能的策略来诱导F-ECS为antigensampling富集在肠上皮细胞接种疫苗的系统经口途径。